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101.
Genetic variation in the 5q31 cytokine gene cluster confers susceptibility to Crohn disease 总被引:24,自引:0,他引:24
Rioux JD Daly MJ Silverberg MS Lindblad K Steinhart H Cohen Z Delmonte T Kocher K Miller K Guschwan S Kulbokas EJ O'Leary S Winchester E Dewar K Green T Stone V Chow C Cohen A Langelier D Lapointe G Gaudet D Faith J Branco N Bull SB McLeod RS Griffiths AM Bitton A Greenberg GR Lander ES Siminovitch KA Hudson TJ 《Nature genetics》2001,29(2):223-228
Linkage disequilibrium (LD) mapping provides a powerful method for fine-structure localization of rare disease genes, but has not yet been widely applied to common disease. We sought to design a systematic approach for LD mapping and apply it to the localization of a gene (IBD5) conferring susceptibility to Crohn disease. The key issues are: (i) to detect a significant LD signal (ii) to rigorously bound the critical region and (iii) to identify the causal genetic variant within this region. We previously mapped the IBD5 locus to a large region spanning 18 cM of chromosome 5q31 (P<10(-4)). Using dense genetic maps of microsatellite markers and single-nucleotide polymorphisms (SNPs) across the entire region, we found strong evidence of LD. We bound the region to a common haplotype spanning 250 kb that shows strong association with the disease (P< 2 x 10(-7)) and contains the cytokine gene cluster. This finding provides overwhelming evidence that a specific common haplotype of the cytokine region in 5q31 confers susceptibility to Crohn disease. However, genetic evidence alone is not sufficient to identify the causal mutation within this region, as strong LD across the region results in multiple SNPs having equivalent genetic evidence-each consistent with the expected properties of the IBD5 locus. These results have important implications for Crohn disease in particular and LD mapping in general. 相似文献
102.
Najmabadi H Hu H Garshasbi M Zemojtel T Abedini SS Chen W Hosseini M Behjati F Haas S Jamali P Zecha A Mohseni M Püttmann L Vahid LN Jensen C Moheb LA Bienek M Larti F Mueller I Weissmann R Darvish H Wrogemann K Hadavi V Lipkowitz B Esmaeeli-Nieh S Wieczorek D Kariminejad R Firouzabadi SG Cohen M Fattahi Z Rost I Mojahedi F Hertzberg C Dehghan A Rajab A Banavandi MJ Hoffer J Falah M Musante L Kalscheuer V Ullmann R Kuss AW Tzschach A Kahrizi K Ropers HH 《Nature》2011,478(7367):57-63
103.
104.
105.
Mediation of Drosophila head development by gap-like segmentation genes 总被引:14,自引:0,他引:14
106.
Glycoprotein C of herpes simplex virus 1 acts as a receptor for the C3b complement component on infected cells 总被引:10,自引:0,他引:10
Receptors for the Fc portion of immunoglobulins or for the third component of complement (C3) are present on a variety of circulating and fixed tissue cells including granulocytes, monocytes, lymphocytes and glomerular epithelial cells. Cells which lack Fc receptors may express them after infection by herpes simplex virus (HSV)-1, HSV-2, cytomegalovirus or varicella zoster virus. We recently reported that infection by HSV-1 induces both Fc and C3 receptors on human endothelial cells. Glycoprotein E of HSV-1 has been shown to function as an Fc receptor. We now demonstrate that glycoprotein C (gC) of HSV-1 functions as a C3b receptor. This receptor appears following HSV-1, but not HSV-2, infection. Detection of the C3b receptor is blocked by monoclonal antibodies to glycoprotein C (gC) of HSV-1, but not by monoclonal antibodies to other HSV-1 glycoproteins. In addition, the MP mutant of HSV-1, which lacks gC, fails to express a C3b receptor. These results assign a new function of gC of HSV-1 and demonstrate potentially important differences between HSV-1 and HSV-2 glycoproteins. 相似文献
107.
M. Prioux-Guyonneau E. Mocaër-Cretet Y. Cohen C. Jacquot 《Cellular and molecular life sciences : CMLS》1984,40(12):1388-1389
Summary Tabernanthine increased the synthesis and elimination of catecholamines (CA) in the striatum and the rest of the brain, but not in the hypothalamus. These data provide evidence that tabernanthine may activate CA turnover of some brain structures by acting at 2 steps of the metabolic pathway. The results are discussed in relation to a central stimulating action and a hypoxia antagonistic effect of this drug.Acknowledgments. Tabernanthine was generously provided by the Institut de Chimie des Substances Naturelles of the C.N.R.S., Gifsur-Yvette, by B. Poiteau, Dat-Xuong, H. P. Husson, Mme Ch. Kan-Fan and P. Potier. 相似文献
108.
A single origin of phenylketonuria in Yemenite Jews 总被引:12,自引:0,他引:12
S Avigad B E Cohen S Bauer G Schwartz M Frydman S L Woo Y Niny Y Shiloh 《Nature》1990,344(6262):168-170
Phenylketonuria (PKU) is a metabolic disease caused by recessive mutations of the gene encoding the hepatic enzyme phenylalanine hydroxylase (PAH). The incidence of PKU varies widely across different geographic areas, and is highest (about 1 in 5,000 live births) in Ireland and western Scotland, and among Yemenite Jews. A limited number of point mutations account for most of the PKU cases in the European population. Here we report that a single molecular defect--a deletion spanning the third exon of the PAH gene--is responsible for all the PKU cases among the Yemenite Jews. Examination of a random sample of Yemenite Jews using a molecular probe that detects the carriers of this deletion indicated a high frequency of the defective gene in this community. Although the deleted PAH gene was traced to 25 different locations throughout Yemen, family histories and official documents of the Yemenite Jewish community showed that the common ancestor of all the carriers of this genetic defect lived in San'a, the capital of Yemen, before the eighteenth century. 相似文献
109.
M Sasportes E Wollman D Cohen D Fradelizi E Carosella G Cathely J Dausset 《Comptes rendus des séances de l'Académie des sciences. Série D, Sciences naturelles》1979,289(1-2):41-46
During the secondary mixed lymphocyte reaction (MLR), i.e. after the double in vitro allogenic sensitization between responding and stimulating cells bearing at least one HLA-DR incompatibility, suppressor cells are developed [1]. They are able to inhibit a primary MLR provided that the stimulating cells possess the same DR incompatibility as the immunizing cells. We report here that this inhibition is due to the production by these cells of a soluble suppressor factor which acts on responding cells provided that they share at least one gene product of the HLA-D region with the cells producing the factor. This a feedback process of auto-inhibition occurring after hyperimmunization. The action of this suppressor factor seems to be genetically restricted to an as yet unknown locus in linkage disequilibrium with HLA-DR. 相似文献